Lipocalin-2 is an essential component of the innate immune response to Acinetobacter baumannii infection
Acinetobacter baumannii is an opportunistic pathogen and an emerging global health threat. Within healthcare settings, major presentations of A . baumannii include bloodstream infections and ventilator-associated pneumonia. The increased prevalence of ventilated patients during the COVID-19 pandemic...
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creator | Sheldon, Jessica R Himmel, Lauren E Kunkle, Dillon E Monteith, Andrew J Maloney, K. Nichole Skaar, Eric P |
description | Acinetobacter baumannii
is an opportunistic pathogen and an emerging global health threat. Within healthcare settings, major presentations of
A
.
baumannii
include bloodstream infections and ventilator-associated pneumonia. The increased prevalence of ventilated patients during the COVID-19 pandemic has led to a rise in secondary bacterial pneumonia caused by multidrug resistant (MDR)
A
.
baumannii
. Additionally, due to its MDR status and the lack of antimicrobial drugs in the development pipeline, the World Health Organization has designated carbapenem-resistant
A
.
baumannii
to be its priority critical pathogen for the development of novel therapeutics. To better inform the design of new treatment options, a comprehensive understanding of how the host contains
A
.
baumannii
infection is required. Here, we investigate the innate immune response to
A
.
baumannii
by assessing the impact of infection on host gene expression using NanoString technology. The transcriptional profile observed in the
A
.
baumannii
infected host is characteristic of Gram-negative bacteremia and reveals expression patterns consistent with the induction of nutritional immunity, a process by which the host exploits the availability of essential nutrient metals to curtail bacterial proliferation. The gene encoding for lipocalin-2 (
Lcn2
), a siderophore sequestering protein, was the most highly upregulated during
A
.
baumannii
bacteremia, of the targets assessed, and corresponds to robust LCN2 expression in tissues.
Lcn2
-/-
mice exhibited distinct organ-specific gene expression changes including increased transcription of genes involved in metal sequestration, such as
S100A8
and
S100A9
, suggesting a potential compensatory mechanism to perturbed metal homeostasis.
In vitro
, LCN2 inhibits the iron-dependent growth of
A
.
baumannii
and induces iron-regulated gene expression. To elucidate the role of LCN2 in infection, WT and
Lcn2
-/-
mice were infected with
A
.
baumannii
using both bacteremia and pneumonia models. LCN2 was not required to control bacterial growth during bacteremia but was protective against mortality. In contrast, during pneumonia
Lcn2
-/-
mice had increased bacterial burdens in all organs evaluated, suggesting that LCN2 plays an important role in inhibiting the survival and dissemination of
A
.
baumannii
. The control of
A
.
baumannii
infection by LCN2 is likely multifactorial, and our results suggest that impairment of iron acquisition by the pathogen is a contribu |
doi_str_mv | 10.1371/journal.ppat.1010809 |
format | Article |
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is an opportunistic pathogen and an emerging global health threat. Within healthcare settings, major presentations of
A
.
baumannii
include bloodstream infections and ventilator-associated pneumonia. The increased prevalence of ventilated patients during the COVID-19 pandemic has led to a rise in secondary bacterial pneumonia caused by multidrug resistant (MDR)
A
.
baumannii
. Additionally, due to its MDR status and the lack of antimicrobial drugs in the development pipeline, the World Health Organization has designated carbapenem-resistant
A
.
baumannii
to be its priority critical pathogen for the development of novel therapeutics. To better inform the design of new treatment options, a comprehensive understanding of how the host contains
A
.
baumannii
infection is required. Here, we investigate the innate immune response to
A
.
baumannii
by assessing the impact of infection on host gene expression using NanoString technology. The transcriptional profile observed in the
A
.
baumannii
infected host is characteristic of Gram-negative bacteremia and reveals expression patterns consistent with the induction of nutritional immunity, a process by which the host exploits the availability of essential nutrient metals to curtail bacterial proliferation. The gene encoding for lipocalin-2 (
Lcn2
), a siderophore sequestering protein, was the most highly upregulated during
A
.
baumannii
bacteremia, of the targets assessed, and corresponds to robust LCN2 expression in tissues.
Lcn2
-/-
mice exhibited distinct organ-specific gene expression changes including increased transcription of genes involved in metal sequestration, such as
S100A8
and
S100A9
, suggesting a potential compensatory mechanism to perturbed metal homeostasis.
In vitro
, LCN2 inhibits the iron-dependent growth of
A
.
baumannii
and induces iron-regulated gene expression. To elucidate the role of LCN2 in infection, WT and
Lcn2
-/-
mice were infected with
A
.
baumannii
using both bacteremia and pneumonia models. LCN2 was not required to control bacterial growth during bacteremia but was protective against mortality. In contrast, during pneumonia
Lcn2
-/-
mice had increased bacterial burdens in all organs evaluated, suggesting that LCN2 plays an important role in inhibiting the survival and dissemination of
A
.
baumannii
. The control of
A
.
baumannii
infection by LCN2 is likely multifactorial, and our results suggest that impairment of iron acquisition by the pathogen is a contributing factor. Modulation of LCN2 expression or modifying the structure of LCN2 to expand upon its ability to sequester siderophores may thus represent feasible avenues for therapeutic development against this pathogen.</description><identifier>ISSN: 1553-7374</identifier><identifier>ISSN: 1553-7366</identifier><identifier>EISSN: 1553-7374</identifier><identifier>DOI: 10.1371/journal.ppat.1010809</identifier><identifier>PMID: 36054235</identifier><language>eng</language><publisher>San Francisco: Public Library of Science</publisher><subject>Acinetobacter baumannii ; Acinetobacter infections ; Animal tissues ; Antiinfectives and antibacterials ; Antimicrobial agents ; Bacteremia ; Bacteria ; Biology and Life Sciences ; Carrier proteins ; COVID-19 ; Disinfection & disinfectants ; Drug development ; Drug resistance ; Gene expression ; Genetic aspects ; Global health ; Health aspects ; Health care ; Health risks ; Heavy metals ; Homeostasis ; Immune response ; Immune system ; Immunosuppressive agents ; Infections ; Innate immunity ; Iron ; Lipocalin ; Medicine and Health Sciences ; Metals ; Multidrug resistance ; Neutrophils ; Nutrient availability ; Opportunist infection ; Pandemics ; Pathogenesis ; Pathogens ; Physical Sciences ; Pneumonia ; Prevention ; Public health ; R&D ; Research & development ; Research and Analysis Methods ; Sequestering ; Siderophores ; Ventilation ; Ventilator-associated pneumonia ; Virulence</subject><ispartof>PLoS pathogens, 2022-09, Vol.18 (9), p.e1010809-e1010809</ispartof><rights>COPYRIGHT 2022 Public Library of Science</rights><rights>2022 Sheldon et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2022 Sheldon et al 2022 Sheldon et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c638t-74acb2c4eaca59cce4957c900763f3a2f4eafaa9de1d7c2c1e575dadc1ad41613</citedby><cites>FETCH-LOGICAL-c638t-74acb2c4eaca59cce4957c900763f3a2f4eafaa9de1d7c2c1e575dadc1ad41613</cites><orcidid>0000-0001-5094-8105</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9477428/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9477428/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79342,79343</link.rule.ids></links><search><creatorcontrib>Sheldon, Jessica R</creatorcontrib><creatorcontrib>Himmel, Lauren E</creatorcontrib><creatorcontrib>Kunkle, Dillon E</creatorcontrib><creatorcontrib>Monteith, Andrew J</creatorcontrib><creatorcontrib>Maloney, K. Nichole</creatorcontrib><creatorcontrib>Skaar, Eric P</creatorcontrib><title>Lipocalin-2 is an essential component of the innate immune response to Acinetobacter baumannii infection</title><title>PLoS pathogens</title><description>Acinetobacter baumannii
is an opportunistic pathogen and an emerging global health threat. Within healthcare settings, major presentations of
A
.
baumannii
include bloodstream infections and ventilator-associated pneumonia. The increased prevalence of ventilated patients during the COVID-19 pandemic has led to a rise in secondary bacterial pneumonia caused by multidrug resistant (MDR)
A
.
baumannii
. Additionally, due to its MDR status and the lack of antimicrobial drugs in the development pipeline, the World Health Organization has designated carbapenem-resistant
A
.
baumannii
to be its priority critical pathogen for the development of novel therapeutics. To better inform the design of new treatment options, a comprehensive understanding of how the host contains
A
.
baumannii
infection is required. Here, we investigate the innate immune response to
A
.
baumannii
by assessing the impact of infection on host gene expression using NanoString technology. The transcriptional profile observed in the
A
.
baumannii
infected host is characteristic of Gram-negative bacteremia and reveals expression patterns consistent with the induction of nutritional immunity, a process by which the host exploits the availability of essential nutrient metals to curtail bacterial proliferation. The gene encoding for lipocalin-2 (
Lcn2
), a siderophore sequestering protein, was the most highly upregulated during
A
.
baumannii
bacteremia, of the targets assessed, and corresponds to robust LCN2 expression in tissues.
Lcn2
-/-
mice exhibited distinct organ-specific gene expression changes including increased transcription of genes involved in metal sequestration, such as
S100A8
and
S100A9
, suggesting a potential compensatory mechanism to perturbed metal homeostasis.
In vitro
, LCN2 inhibits the iron-dependent growth of
A
.
baumannii
and induces iron-regulated gene expression. To elucidate the role of LCN2 in infection, WT and
Lcn2
-/-
mice were infected with
A
.
baumannii
using both bacteremia and pneumonia models. LCN2 was not required to control bacterial growth during bacteremia but was protective against mortality. In contrast, during pneumonia
Lcn2
-/-
mice had increased bacterial burdens in all organs evaluated, suggesting that LCN2 plays an important role in inhibiting the survival and dissemination of
A
.
baumannii
. The control of
A
.
baumannii
infection by LCN2 is likely multifactorial, and our results suggest that impairment of iron acquisition by the pathogen is a contributing factor. Modulation of LCN2 expression or modifying the structure of LCN2 to expand upon its ability to sequester siderophores may thus represent feasible avenues for therapeutic development against this pathogen.</description><subject>Acinetobacter baumannii</subject><subject>Acinetobacter infections</subject><subject>Animal tissues</subject><subject>Antiinfectives and antibacterials</subject><subject>Antimicrobial agents</subject><subject>Bacteremia</subject><subject>Bacteria</subject><subject>Biology and Life Sciences</subject><subject>Carrier proteins</subject><subject>COVID-19</subject><subject>Disinfection & disinfectants</subject><subject>Drug development</subject><subject>Drug resistance</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Global health</subject><subject>Health aspects</subject><subject>Health care</subject><subject>Health risks</subject><subject>Heavy metals</subject><subject>Homeostasis</subject><subject>Immune response</subject><subject>Immune system</subject><subject>Immunosuppressive agents</subject><subject>Infections</subject><subject>Innate immunity</subject><subject>Iron</subject><subject>Lipocalin</subject><subject>Medicine and Health Sciences</subject><subject>Metals</subject><subject>Multidrug resistance</subject><subject>Neutrophils</subject><subject>Nutrient availability</subject><subject>Opportunist infection</subject><subject>Pandemics</subject><subject>Pathogenesis</subject><subject>Pathogens</subject><subject>Physical Sciences</subject><subject>Pneumonia</subject><subject>Prevention</subject><subject>Public health</subject><subject>R&D</subject><subject>Research & development</subject><subject>Research and Analysis Methods</subject><subject>Sequestering</subject><subject>Siderophores</subject><subject>Ventilation</subject><subject>Ventilator-associated pneumonia</subject><subject>Virulence</subject><issn>1553-7374</issn><issn>1553-7366</issn><issn>1553-7374</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqVkkuP0zAQxyMEYpeFb4BEJC5waPEzbi5I1YpHpQokHmdrMpm0XiV2iZ0VfHtcGhBFe0E--DG_-dvz9xTFU86WXBr-6iZMo4d-eThAWnLG2YrV94pLrrVcGGnU_b_WF8WjGG8YU1zy6mFxISumlZD6sthv3SEg9M4vROliCb6kGMknB32JYTgEnzdl6Mq0p9J5DylPwzB5KkeKORypTKFco_OUQgOYaCwbmAbw3rmc0REmF_zj4kEHfaQn83xVfH375sv1-8X247vN9Xq7wEqu0sIowEagIkDQNSKpWhusGTOV7CSILkc6gLol3hoUyEkb3UKLHFrFKy6vimcn3UMfop1NilYYoYWRSspMbE5EG-DGHkY3wPjDBnD210EYdxbG5LAnqyqqVlq2YtUYpTU1jYAKlRTYkDCaZa3X821TM1CL2asR-jPR84h3e7sLt7ZWxiixygIvZoExfJsoJju4iNT34ClMx3ez2kjNuMjo83_Qu6ubqR3kArL9Id-LR1G7NoJlt3KvZGp5B5VHS4PD_Oedy-dnCS_PEjKT6HvawRSj3Xz-9B_sh3NWnVgcQ4wjdX-848we-_x3kfbY53buc_kTqxXwXQ</recordid><startdate>20220902</startdate><enddate>20220902</enddate><creator>Sheldon, Jessica R</creator><creator>Himmel, Lauren E</creator><creator>Kunkle, Dillon E</creator><creator>Monteith, Andrew J</creator><creator>Maloney, K. Nichole</creator><creator>Skaar, Eric P</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>AAYXX</scope><scope>CITATION</scope><scope>ISN</scope><scope>ISR</scope><scope>3V.</scope><scope>7QL</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>COVID</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0001-5094-8105</orcidid></search><sort><creationdate>20220902</creationdate><title>Lipocalin-2 is an essential component of the innate immune response to Acinetobacter baumannii infection</title><author>Sheldon, Jessica R ; Himmel, Lauren E ; Kunkle, Dillon E ; Monteith, Andrew J ; Maloney, K. Nichole ; Skaar, Eric P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c638t-74acb2c4eaca59cce4957c900763f3a2f4eafaa9de1d7c2c1e575dadc1ad41613</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Acinetobacter baumannii</topic><topic>Acinetobacter infections</topic><topic>Animal tissues</topic><topic>Antiinfectives and antibacterials</topic><topic>Antimicrobial agents</topic><topic>Bacteremia</topic><topic>Bacteria</topic><topic>Biology and Life Sciences</topic><topic>Carrier proteins</topic><topic>COVID-19</topic><topic>Disinfection & disinfectants</topic><topic>Drug development</topic><topic>Drug resistance</topic><topic>Gene expression</topic><topic>Genetic aspects</topic><topic>Global health</topic><topic>Health aspects</topic><topic>Health care</topic><topic>Health risks</topic><topic>Heavy metals</topic><topic>Homeostasis</topic><topic>Immune response</topic><topic>Immune system</topic><topic>Immunosuppressive agents</topic><topic>Infections</topic><topic>Innate immunity</topic><topic>Iron</topic><topic>Lipocalin</topic><topic>Medicine and Health Sciences</topic><topic>Metals</topic><topic>Multidrug resistance</topic><topic>Neutrophils</topic><topic>Nutrient availability</topic><topic>Opportunist infection</topic><topic>Pandemics</topic><topic>Pathogenesis</topic><topic>Pathogens</topic><topic>Physical Sciences</topic><topic>Pneumonia</topic><topic>Prevention</topic><topic>Public health</topic><topic>R&D</topic><topic>Research & development</topic><topic>Research and Analysis Methods</topic><topic>Sequestering</topic><topic>Siderophores</topic><topic>Ventilation</topic><topic>Ventilator-associated pneumonia</topic><topic>Virulence</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sheldon, Jessica R</creatorcontrib><creatorcontrib>Himmel, Lauren E</creatorcontrib><creatorcontrib>Kunkle, Dillon E</creatorcontrib><creatorcontrib>Monteith, Andrew J</creatorcontrib><creatorcontrib>Maloney, K. Nichole</creatorcontrib><creatorcontrib>Skaar, Eric P</creatorcontrib><collection>CrossRef</collection><collection>Gale In Context: Canada</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>Coronavirus Research Database</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PLoS pathogens</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sheldon, Jessica R</au><au>Himmel, Lauren E</au><au>Kunkle, Dillon E</au><au>Monteith, Andrew J</au><au>Maloney, K. Nichole</au><au>Skaar, Eric P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Lipocalin-2 is an essential component of the innate immune response to Acinetobacter baumannii infection</atitle><jtitle>PLoS pathogens</jtitle><date>2022-09-02</date><risdate>2022</risdate><volume>18</volume><issue>9</issue><spage>e1010809</spage><epage>e1010809</epage><pages>e1010809-e1010809</pages><issn>1553-7374</issn><issn>1553-7366</issn><eissn>1553-7374</eissn><abstract>Acinetobacter baumannii
is an opportunistic pathogen and an emerging global health threat. Within healthcare settings, major presentations of
A
.
baumannii
include bloodstream infections and ventilator-associated pneumonia. The increased prevalence of ventilated patients during the COVID-19 pandemic has led to a rise in secondary bacterial pneumonia caused by multidrug resistant (MDR)
A
.
baumannii
. Additionally, due to its MDR status and the lack of antimicrobial drugs in the development pipeline, the World Health Organization has designated carbapenem-resistant
A
.
baumannii
to be its priority critical pathogen for the development of novel therapeutics. To better inform the design of new treatment options, a comprehensive understanding of how the host contains
A
.
baumannii
infection is required. Here, we investigate the innate immune response to
A
.
baumannii
by assessing the impact of infection on host gene expression using NanoString technology. The transcriptional profile observed in the
A
.
baumannii
infected host is characteristic of Gram-negative bacteremia and reveals expression patterns consistent with the induction of nutritional immunity, a process by which the host exploits the availability of essential nutrient metals to curtail bacterial proliferation. The gene encoding for lipocalin-2 (
Lcn2
), a siderophore sequestering protein, was the most highly upregulated during
A
.
baumannii
bacteremia, of the targets assessed, and corresponds to robust LCN2 expression in tissues.
Lcn2
-/-
mice exhibited distinct organ-specific gene expression changes including increased transcription of genes involved in metal sequestration, such as
S100A8
and
S100A9
, suggesting a potential compensatory mechanism to perturbed metal homeostasis.
In vitro
, LCN2 inhibits the iron-dependent growth of
A
.
baumannii
and induces iron-regulated gene expression. To elucidate the role of LCN2 in infection, WT and
Lcn2
-/-
mice were infected with
A
.
baumannii
using both bacteremia and pneumonia models. LCN2 was not required to control bacterial growth during bacteremia but was protective against mortality. In contrast, during pneumonia
Lcn2
-/-
mice had increased bacterial burdens in all organs evaluated, suggesting that LCN2 plays an important role in inhibiting the survival and dissemination of
A
.
baumannii
. The control of
A
.
baumannii
infection by LCN2 is likely multifactorial, and our results suggest that impairment of iron acquisition by the pathogen is a contributing factor. Modulation of LCN2 expression or modifying the structure of LCN2 to expand upon its ability to sequester siderophores may thus represent feasible avenues for therapeutic development against this pathogen.</abstract><cop>San Francisco</cop><pub>Public Library of Science</pub><pmid>36054235</pmid><doi>10.1371/journal.ppat.1010809</doi><tpages>e1010809</tpages><orcidid>https://orcid.org/0000-0001-5094-8105</orcidid><oa>free_for_read</oa></addata></record> |
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source | DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; PubMed Central Open Access; Public Library of Science (PLoS) |
subjects | Acinetobacter baumannii Acinetobacter infections Animal tissues Antiinfectives and antibacterials Antimicrobial agents Bacteremia Bacteria Biology and Life Sciences Carrier proteins COVID-19 Disinfection & disinfectants Drug development Drug resistance Gene expression Genetic aspects Global health Health aspects Health care Health risks Heavy metals Homeostasis Immune response Immune system Immunosuppressive agents Infections Innate immunity Iron Lipocalin Medicine and Health Sciences Metals Multidrug resistance Neutrophils Nutrient availability Opportunist infection Pandemics Pathogenesis Pathogens Physical Sciences Pneumonia Prevention Public health R&D Research & development Research and Analysis Methods Sequestering Siderophores Ventilation Ventilator-associated pneumonia Virulence |
title | Lipocalin-2 is an essential component of the innate immune response to Acinetobacter baumannii infection |
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